摘要:
本文采用基于密度泛函理论(DFT)框架下广义梯度近似平面波超软赝势法，支气管哮喘是一种全球性的发病率日益升高的呼吸道变应性疾病，支气管哮喘严重影响儿童的生长发育和心理健康，甚至威胁到他们的生命。但其发病机制目前尚未完全阐明，传统的观点认为Th1/Th2平衡失调理论在哮喘的发病中起着重要的作用。但随着对Th1，Th2以外的其他T细胞亚群的研究，人们逐渐发现CD4+CD25+Treg细胞与哮喘有着密切的关系。而糖皮质激素诱导的肿瘤坏死因子受体(Glucocorticoid-induced tumor necrosis factor receptor GITR)是属于肿瘤坏死因子受体(Tumor necrosis factor receptor TNFR)超家族的成员之一，在CD4+CD25+T调节细胞(Regulatory T cell Treg)细胞高表达，与其配体糖皮质激素诱导的肿瘤坏死因子受体配体(Glucocorticoid-induced tumor necrosis factor receptor ligand GITRL)结合后能增强T细胞激活、增殖、分泌细胞因子、MAPKs和NF-κB激活效应、抑制CD4+CD25+Treg细胞的功能，从而加强效应性T细胞的活性，有利于增强抗肿瘤免疫和抗病毒免疫，在免疫系统的调节中起着复杂的作用。
Bronchial asthma is a global respiratory allergic disease, with the rising incidence of bronchial asthma in children. It has seriously affected children’s growth and mental health, and even may be life-threatening. But its pathogenesis has not fully elucidated so far, and the traditional view is that the disorder of Th1/Th2 balance plays an important role in the onset of asthma. But with the study of other T cell subsets besides Th1 and Th2, we gradually find that there exists a close relationgship between CD4+CD25+ Regulatory T cell (Treg) and asthma. Glucocorticoid-induc- ed tumor necrosis factor receptor (GITR) is one member of Tumor necrosis factor receptor (TNFR) superfamily, and is highly expressed in CD4+CD25+ Treg. When combining with its ligand GITRL (Glucocorticoid-induced tumor necrosis factor receptor ligand). They can not only enhance the activation and proliferation of T cell, enhance the effect of MAPKs and NF-κB, but also inhibit the function of CD4+CD25+ Treg cells. GITR/GITRL signal is beneficial to antitumor immune and antiviral immunity and plays a complex role in the regulation of the immune system.